PROJECT SUMMARY/ABSTRACT In recognition of the developmental heterogeneity of ASD, Miles and colleagues divided ASD into two groups: complex autism and essential autism. The label complex autism grouped together children with ASD who had overt evidence of abnormalities of early morphogenesis, e.g. as signaled by the presence of multiple dysmorphic features and/or microcephaly and associated with lower IQs, more seizures, and higher incidence of EEG and MRI abnormalities. Children with essential autism, by comparison, had fewer dysmorphic features, had greater male to female ratios, and showed greater heritability of autism features within families. An implication of this work was that in complex autism, autism was expected to arise as the result of broad developmental insult that also impacted social function, whereas essential autism was viewed as the result of specific social neural systems dysfunction. In this study, we use this conceptualization of complex versus essential autism to longitudinally track from 6 to 36 months of age two groups of infants with distinct etiologies but common elevation of autism symptoms: very low birthweight (VLBW, n=100) infants, who, like children with complex autism, are expected to evidence a broad range of delays in multiple domains, and high-risk infant siblings of children with ASD (HR-Sibs, n=100), who, as in essential autism, show heightened heritability of ASD symptoms and greater risk for social and communicative challenges. These groups are compared against a control group of low-risk typically developing children (LR, n=100). We take promising eye tracking (ET) and EEG paradigms that have been associated with the emergence of ASD in HR-Sibs in the first year after life after birth, and which were primarily developed to capture social dimensions of function, and extend them in order to investigate analogous nonsocial information processing. We hypothesize that VLBW infants evidencing ASD symptoms will show decreased performance in both social and nonsocial tasks, highlighting generalized difficulty with information processing consistent with broader developmental risk, whereas we hypothesize that difficulties in HR-Sibs with similar ASD symptoms will show more specific social (c.f. nonsocial) atypicalities. By adapting and extending paradigms which have shown strong or unique signal for later ASD in HR-Sibs, we will further our understanding of mechanisms underlying ASD risk and inform potential biomarker discovery; by pairing this with different etiological risk groups, we will elucidate multilevel vulnerabilities that can shape developmental trajectories and the emergence of the disorder. In summary, this work will advance our understanding of developmental trajectories of risk associated with ASD, elucidate mechanisms underlying later emergence of core autism features, and help to test and refine the sensitivity and specificity of putative early neurobehavioral and neurocognitive biomarkers for ASD.